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PubMed2005

Early low-grade proteinuria: causes, short-term evolution and long-term consequences in renal transplantation.

Proteinuria 1 year after transplantation is associated with poor renal outcome. It is unclear whether low-grade (<1 g/24 h) proteinuria earlier after transplantation and its short-term change affect long-term graft survival. The effects of proteinuria and its change on long-term graft survival were retrospectively assessed in 484 renal transplant recipients. One- and 3-month proteinuria correlated with donor age, donor cardiovascular death, prolonged cold and warm ischemia times and acute rejection. One- and 3-month proteinuria (per 0.1 g/24 h, hazard ratio (HR): 1.07 and 1.15, p<0.0001)-especially low-grade proteinuria (HR: 1.20 and 1.26, p<0.0001)-were powerful, independent predictors of graft loss. Its short-term reduction correlated with arterial pressure (AP) (the lower the 3-month diastolic and 12-month systolic AP, the lower the risk of increasing proteinuria during 1-3 months and 3-12 months periods, respectively: Odds ratio (OR) per 10 MmHg: 0.78, p=0.01 and 0.85, respectively, p=0.02), and was associated with decreased long-term graft loss (per 0.1 g/24 h: HR: 0.88 and 0.98, respectively, p<0.0001), independently of initial proteinuria. Early low-grade proteinuria due to pre-transplant renal lesions, ischemia-reperfusion and immunologic injuries is a potent predictor of graft loss. Short-term reduction in proteinuria is associated with improved long-term graft survival.

Adult↗
PubMed2005

Diabetic nephropathy: the proteinuria hypothesis.

BACKGROUND/AIMS: Proteinuria, nearly a universal finding in progressive kidney disease, has been the subject of frequent recent analyses in the renal literature. Proteinuria is a hallmark of diabetic nephropathy: microalbuminuria is the principal early predictor for progression of diabetic glomerulopathy, and proteinuria may be viewed as a measure of the severity and promoter of progression of nephropathy. METHODS: This article critically reviews for the first time the full scope of diabetic proteinuria--complex molecular mechanisms, natural history, and analysis of treatment trials--in order to address the validity of 'the proteinuria hypothesis', i.e., that diabetic proteinuria is a modifiable determinant of renal progression. This hypothesis is analyzed in detail, including recent studies on the primary therapy of diabetic nephropathy, renin-angiotensin blockade. RESULTS: As fully developed, this hypothesis consists of three postulates: that higher amounts of proteinuria predict progressive loss of function, that proteinuria reduction correlates with slowing progression, and that proteinuria is a surrogate endpoint for clinical trials. The latter postulate has not before been adequately linked to growing information about the first two postulates as they apply to diabetic kidney disease. CONCLUSION: While diabetic nephropathy is a disease model for the potential use of proteinuria as a surrogate marker for renal progression, this shift in perspective will require prospective data from additional clinical trials, particularly of non-renin-angiotensin blocking drugs, to be complete.

Diabetic Nephropathies↗
PubMed2006

Biphasic pattern of exercise-induced proteinuria in sedentary and trained men.

BACKGROUND/AIMS: Exercise-induced proteinuria is a common consequence of physical activity, although its mechanism is not clear. Oxidant stress has been proposed as one of different factors involved in postexercise proteinuria in rats. In this study we investigated whether reactive oxygen radicals generated during exercise play a role in exercise-induced proteinuria in sedentary and trained men. METHODS: The validity of oxidant stress following stepwise maximal exercise on proteinuria was investigated in sedentary and trained subjects before and after antioxidant vitamin treatment (A, C, and E) for 2 months. While protein carbonyl content in serum and thiobarbituric acid reactive substances (TBARS) in erythrocytes and urine were used as oxidant stress markers, total protein, albumin, beta(2)-microglobulin in urine were assayed for proteinuria in five consecutive specimens after exercise. Urines were collected before exercise, then 30 min, 2, 8 and 24 h postexercise. RESULTS: Increased urinary protein levels and mixed type proteinuria were determined after 30 min of exercise in sedentary and trained subjects. Proteinuria was normalized at 2 and 8 h specimens. However, glomerular type proteinuria was identified at 24 h specimen in both groups. Oxidant stress markers were significantly elevated in sedentary and trained subjects. Antioxidant treatment prevented the increase in oxidant stress markers, urinary protein levels and the occurrence of glomerular type proteinuria after exhaustive exercise at 24 h in both groups. CONCLUSIONS: These findings suggest that the exercise-induced oxidant stress may contribute to exercise-induced proteinuria in sedentary and trained men.

Adult↗
PubMed1995

Induction of proteinuria by adriamycin or bovine serum albumin in the mouse.

To establish models of proteinuria in the mouse, BALB/c mice were injected with puromycin aminonucleoside (PAN, 1.5 or 4.5 mg/10 g body weight), adriamycin (AD, 0.2 mg/10 g body weight) intravenously or bovine serum albumin (BSA, 100 mg/10 g body weight) intraperitoneally. Proteinuria was measured as the ratio of urinary albumin (micrograms/ml) to creatinine (mg/dl) and further characterized by isotyping the immunoglobulin. Although not obtained with PAN (followed for 4 weeks), proteinuria was readily attained in the mouse after treatment with AD or BSA. Most AD-treated mice (5/7) developed an abrupt increase of proteinuria at day 2 after injection, with the ratio of urinary albumin to creatinine in the range 0.28-0.45. The degree of proteinuria increased with time and all mice tested (7/7) showed overt proteinuria at day 4. These mice became anuric at day 5 and died at days 6 and 7. For BSA, 4 h after administration, four of seven mice showed enhanced proteinuria, lasting 8 h with urinary albumin and creatinine in a ratio < 0.05. Isotyping of urine samples collected at the time of heavy proteinuria (ratio of urinary albumin to creatinine: > 0.40 for AD-treated mice, > 0.15 for BSA-treated mice) showed that all of the mice (7/7) with AD-induced proteinuria (ADp) and three of four mice with BSA-induced proteinuria (BSAp) revealed urinary IgG2b and IgA, while only one of seven control mice showed IgG2b alone in urine. The mice were sacrificed at the time they presented with heavy proteinura for pathologic and anionic studies on renal tissues.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Proteinuria and vascular changes after renal irradiation: the role of reactive oxygen species (ROS) and vascular endothelial growth factor (Vegf).

Proteinuria occurs in all degrees of radiation nephropathy and can be present without other symptoms. In this study, radiation-induced proteinuria in C3H mice demonstrated a clear dose-response relationship and was apparent before the onset of significant structural vascular changes and decreases in renal function. This suggests that proteinuria is not a secondary event due to loss of the vascular structure. In an attempt to ameliorate radiation-induced proteinuria and progressive renal failure, two factors were studied. The influence of reactive oxygen species (ROS), which are generated by infiltrating neutrophils and mediate proteinuria in models of acute glomerular injury, was the first to be investigated. Short-term administration of the reactive oxygen scavengers superoxide dismutase (SOD) and catalase did not reverse an established radiation-induced proteinuria. Continuous administration of the antioxidant N-acetylcysteine (NAC) also failed to inhibit this proteinuria. However, since no direct assessment of the impact of these interventions on renal redox status was made, the putative role of ROS in radiation-induced proteinuria and nephropathy remains undefined. The second factor studied was vascular endothelial growth factor (Vegf), which is suggested to be involved in glomerular vessel permeability and the development of proteinuria in some models of renal disease. Northern blot analysis of mRNA from whole kidneys did not demonstrate any increased expression of Vegf after irradiation. There was also no change in the ratio of the different Vegf isoforms (PCR analysis), either in the whole kidney or in isolated glomeruli. No significant role for Vegf was identified for radiation-induced vascular changes or proteinuria, although post-transcriptional changes cannot be excluded.

Angiogenesis Inducing Agents↗
PubMed1991

Reactive oxygen metabolites cause massive, reversible proteinuria and glomerular sieving defect without apparent ultrastructural abnormality.

To identify the specific in vivo renal effect of reactive oxygen species (ROS), hydrogen peroxide (H2O2) was infused directly into the left renal artery in Munich-Wistar rats. H2O2 (5 to 50 mumol over 1 h) induced a dose-dependent increase in urine protein excretion rate in infused kidneys, reaching a maximum at the dose of 35 mumol (on average, a 60-fold increase from baseline). The H2O2 (35 mumol)-induced proteinuria peaked over 1 h and completely normalized by 24 h after the infusion. Electrophoresis revealed that the urine protein is primarily of glomerular origin. Fractional clearances of graded-size neutral dextran of larger molecular radii, an index of glomerular size selectivity, were significantly and substantially elevated immediately but normalized by 24 h after the infusion. GFR and RPF rate remained unchanged throughout the entire time course examined. The H2O2-induced proteinuria was largely prevented by pretreatment with catalase (20 mg, iv) or deferoxamine (30 mg/100 g body wt, iv). Thus, iron-dependent metabolites of hydrogen peroxide appear to be involved in this proteinuria and glomerular size-selective defect. Light and electron microscopy, including determination of anionic site density at lamina rara externa of glomerular capillary wall by polyethyleneimine staining, did not reveal any appreciable abnormality throughout the study period, including at the peak of proteinuria. Thus, ROS can cause massive, reversible proteinuria by inducing a molecular size-selectivity defect of the glomerular capillary wall without apparent ultrastructural abnormalities. The results raise the possibilities: (1) that persistent proteinuria of a variety of renal diseases may reflect persistence of pathogenic ROS acting on glomeruli because the potent proteinuric effect of ROS can be transient (2) that the light and electron microscopy abnormalities in glomeruli of ROS-induced renal injuries reported thus far may have no direct causal linkage to proteinuria; and, finally, (3) ROS-induced reversible proteinuria may relate to the mechanism of clinical functional proteinuria, which involves increased oxygen and ROS metabolism, e.g., exercise-induced proteinuria.

Animals↗
PubMed1981

Prevalence and causes of proteinuria in 20-year-old Finnish men.

The prevalence and causes of proteinuria were studied in a cohort of 36147 men aged 20 (born in 1956). Proteinuria was found in 139 men (0.4%) at the initial screening or examination. Further investigations reduced the number of proteinuria cases to 72 (0.2%). Persistent proteinuria was demonstrated in 46 men (0.13% of the series) and orthostatic proteinuria in 26 (0.07%). Urography revealed anomalies in 18 of 104 cases. Elevated blood pressure and reduced glomerular filtration rate were observed in a few men, mainly from the group with persistent proteinuria. Renal biopsy was performed in 61 cases--38 with persistent proteinuria, 12 with orthostatic proteinuria and 11 without proteinuria at the time of examination. Light microscopy gave normal findings or showed only slight mesangial or focal glomerulonephritis in the great majority of cases. Membranous, mesangiocapillary or chronic proliferative glomerulonephritis was present in one-fourth of the men with persistent proteinuria. This was the only group with such lesions.

Adult↗
PubMedDate not supplied

[Composition of proteinuria in primary glomerulonephritides: association with tubolo-interstitial damage, outcome and response to therapy].

Experimental and clinical studies show that proteinuria is an independent risk factor for the progression of chronic glomerular diseases and is associated with the extent of tubulo-interstitial damage. The accumulation of proteins in tubular cells induces the increased expression of a variety of inflammatory and fibrogenic cytokines, with the consequent development of interstitial inflammation, a proliferation of fibroblasts, the increased production of extracellular matrix, and the formation of interstitial fibrosis. Laboratory methods, such as immunonephelometry, can easily evaluate the glomerular component of proteinuria, due to the alteration of the structural integrity of the glomerular capillary wall. This alteration allows the tubular lumen to pass proteins of high and middle molecular weight (HMW and MMW proteins: IgM, alpha2-macroglobulin, IgG, transferrin, albumin). Using the same method and SDS-PAGE, it is possible to evaluate those tubular components of proteinuria that are composed of low molecular weight (LMW) proteins, such as alpha1-microglobulin (alpha1m) and beta2-microglobulin (beta2m), whose reabsorption by tubular cells-almost complete in physiological conditions-is impaired in pathological conditions. Recent studies clarified some aspects of the relationships between the components of proteinuria, histological lesions, prediction of outcome, and response to therapy. The extent of tubulo-interstitial damage is correlated with selectivity of proteinuria and IgG excretion, suggesting a possible tubulo-toxic role for IgG or for some other protein of similar molecular weight. The tubulo-interstitial lesions are also correlated with the excretion of LMW proteins, due to their impaired reabsorption. The remission of nephrotic syndrome, not predicted by the amount of proteinuria, is highly predicted by the selectivity index or IgG excretion in membranous glomerulonephritis (MGN) and focal segmental glomerulosclerosis (FSGS). Progression to chronic renal failure is better predicted both by the glomerular component (selectivity index, IgG excretion) and by the tubular component of proteinuria (alpha1m, beta1m, LMW proteins), than by 24-hour proteinuria. The response to therapy in MGN and FSGS is dependent on the excretion of IgG and alpha1m. In conclusion the composition of proteinuria can easily be assessed using automated methods, and it is useful to evaluate the relationship of proteinuria with histological lesions to predict the functional outcome and response to therapy in primary glomerulonephritis.

Electrophoresis, Polyacrylamide Gel↗
PubMed1989

Circadian rhythm of proteinuria: consequences of the use of urinary protein:creatinine ratios.

Proteinuria in patients with glomerular disease has a circadian rhythm, but for creatinine such a rhythm is either absent or of low amplitude. We found in 18 of 23 admitted patients (group I) and in seven outpatients (group II) a marked circadian rhythm of the protein: creatinine ratio. Estimates of 24-h proteinuria were obtained by multiplying the protein:creatinine ratio of 3-h urine samples with 24-h creatinine excretion, calculated from age, sex and bodyweight. Estimated proteinuria could be as low as 19% or as high as 349% of actually measured 24-h proteinuria; the mean SD was 23%. The best estimate was obtained with the 06.00-09.00 hours urine samples. The estimates correlated better with actually measured 24-h proteinuria than the protein: creatinine ratio per se correlated with the 24-h proteinuria. Day-to-day variation of proteinuria estimates from samples taken at the same time of the day was of similar magnitude as day-to-day variation of actual 24-h proteinuria. We conclude that the usefulness of the protein: creatinine ratio of a random urine sample for estimation of proteinuria is limited, because of the circadian rhythm of proteinuria. However, samples collected at a fixed time of the day are an acceptable alternative for 24-h urine collections in the clinical follow-up of individual patients.

Adolescent↗
PubMed1989

Current concepts in proteinuria.

Proteinuria, long recognized as a sign of renal disease, is a common laboratory abnormality in children and adults. Proteinuria may be transient or persistent; when persistent, the cause must be determined. Proteinuria may be primarily glomerular or tubular in origin. Glomerular proteinuria is usually an important concern. Tubular proteinuria often indicates the presence of tubulointerstitial or obstructive renal disease. Screening tests are available to detect albumin (the major protein in glomerular proteinuria), but there are no simple tests for immunoglobulin light chains and low-molecular-mass proteins, which predominate in overflow proteinuria and tubular proteinuria. These small proteins can only be detected by more sophisticated assays such as electrophoresis, isoelectric focusing, and chromatography. The association of glomerular and tubular types of proteinuria with specific disorders is reviewed in this paper, and current concepts in laboratory methodology for the study of proteinuria are summarized.

Humans↗
PubMed1977

Glomerular lesions in patients with asymptomatic persistent andorthostatic proteinuria discovered on routine medical examination.

The incidence of asymptomatic proteinuria in young healthy men entering the army service in Singapore was 0.94%; 0.56% had intermittent orthostatic proteinuria and 0.38% with persistent proteinuria. Renal biopsies from 45 cases with persistent proteinuria and 10 cases with orthostatic proteinuria were studied by light microscopy, electron microscopic and immunofluorescent antibody techniques. Three cases with orthostatic proteinuria showed a minimal lesion ('Nil'), and 7 a minimal lesion with increased centrilobular mesangial matrix and mild focal and segmental mesangial hypercellularity. Focal and segmental capillary loop changes were seen in two cases. No immunoglobulin deposits were found in orthostatic proteinuria. A raised anti-streptolysin O titer was found in 3 cases. 13.3% of cases with persistent proteinuria showed a minimal lesion ('Nil'); 66.6% a minimal lesion with increased centrilobular mesangial matrix and mild focal and segmental mesangial hypercellularity: Focal global sclerosis, focal segmental sclerosing glomerulonephritis and diffuse proliferative GN (mesangial hypercellularity) were each found in 6.7% of patients in this group. Focal and segmental changes in capillary loops were found in 30% of cases. Changes in visceral epithelium such as the appearance of cytoplasmic swelling, vesicles and dense aggregates, and areas of focal foot process fusion were common findings. Mesangial deposits of IgA were found in 34.3%, with an IgA-IgG-beta1C globulin combination in 28.6% of cases. IgM-beta1C globulin was present in 5.7% of cases with persistent proteinuria. Early complement components, C1q and C4, and IgA secretory piece were absent. A raised antistreptolysin O titer was found in 25% of cases. The changes inthe glomeruli may represent the end or healing stages of an early bout of glomerulonephritis. Changed hemodynamic responses on assuming an upright position may play a role in the loss of protein across the glomerular basement membrane in patients with orthostatic proteinuria.

Adolescent↗
PubMed1985

Nephrotic range proteinuria--a good predictive index of disease in IgA nephropathy?

A combined retrospective and prospective study of 86 patients with IgA nephropathy was conducted to determine whether the level of proteinuria was a good predictive index of progressive disease. The patients fell into three groups: Group A, 31 patients with proteinuria of less than 1 g/day, Group B, 31 patients with proteinuria of 1 to 3.5 g/day; and Group C, 24 patients with proteinuria of more than 3.5 g/day. The groups are comparable in age of presentation, sex ratio, and duration of study and showed no difference in serum creatinine levels, creatinine clearance, incidence of hypertension or incidence of impaired renal function. Compared with the patients in the other groups, those in Group C did not have increased incidence of progressive disease. Nevertheless, they have a higher incidence of nephrotic syndrome (p less than 0.001), a lower incidence of macroscopic haematuria (p less than 0.05), lower serum albumin (p less than 0.05) and heavier proteinuria (p less than 0.01). Severity of proteinuria had no significant correlation with the severity of renal histopathologic changes. Clinical observations divided the 24 patients with nephrotic range proteinuria into three well-defined groups with different prognoses. Six patients had progressive disease with decreasing proteinuria. Five of these remained hypertensive and their initial renal biopsy showed advanced pathologic changes. Thirteen patients had persistent proteinuria although the renal function remained unchanged. Three of these were treated with steroid but failed to respond, and their renal histopathologic changes were usually moderate. The remaining five patients showed good response to steroid treatment although two became steroid-dependent. Their renal histopathology showed mild alteration. Our findings suggest that severe proteinuria in IgA nephropathy does not inevitably indicate a poor prognosis.

Adolescent↗
PubMed1979

Diagnostic significance of SDS-PAA-electrophoresis of urinary proteins: different forms of proteinuria and their correlation to renal diseases.

Different types of urinary protein excretion may be recognized by determination of the proteins molecular weight. Beside chromatography different electrophoretic procedures have been applied to urinary proteins to study the underlying renal disease. The various zone electrophoreses separate merely by surface charge, proteins however covered by sodium dodecyl sulfate (SDS) migrate according to their molecular radius. So by SDS-polyacrylamide electrophoresis (SDS-PAe) macromolecular proteinurias (Mr 60,000- greater than 300,000 daltons) due to glomerular damage may be distinguished from micromolecular forms (Mr 10,000-70,000 d) due to tubular dysfunction. By densitometric quantitation of the separated Ig and transferrin an index of the glomerular selectivity is obtained, i.e. the capacity of the glomerular system, to retain serum proteins of a Mr above 150,000 d. By this procedure proliferative and degenerative glomerulopathies may be distinguished from minimal change disease, focal glomerular sclerosis and early membranous nephropathy; serial determinations of this selectivity index in the latter two disease entities show a gradual deterioration of glomerular protein handling with time. A glomerular proteinuria of even "physiological" quantity has been proved as early sign of renal involvment in systemic diseases; it may be detected earlier as for example the retinopathy in juvenile diabetics. Micromolecular proteinurias also occur at least in two forms: the typical tubular proteinuria (MW 10,000-70,000 d) is associated with acute or chronic severe tubular dysfunction as in interstitial nephritis and acute kidney failure; rejection episodes of kidney transplants lead to transient tubular proteinurias, too. The second form of micromolecular proteinuria (Mr 40,000-70,000 d) has been found frequently in association with a glomerular in diabetic and hypertensive glomerulosclerosis. By measuring clearances of the microproteins, the proteinuria with this pattern could be established as form independant from glomerular and tubular proteinurias. The constancy of the two micromolecular proteinurias led to the hypothesis of at least two selective mechanism of tubular protein resorption. SDS-PAe additionally allows the differentiation of extrarenal proteinurias, as caused by overflow, paraproteins, postrenal Ig-secretion or bleeding etc. In comparing clinical and in part histological data of about 2,000 patients suffering from kidney diseases the analysis of urinary proteins by this method has been proved as valuable non-invasive tool for diagnosis and follow-up.

Electrophoresis, Polyacrylamide Gel↗
PubMed2006

Mycophenolate mofetil is effective in reducing lupus glomerulonephritis proteinuria.

Mycophenolate mofetil (MMF) significantly reduces proteinuria in experimental model of human membranous nephropathy (Heymann nephritis). Twenty consecutive SLE patients with persistent isolated severe proteinuria and/or proteinuric flare were studied for 18 months of MMF therapy. All of them presented stable renal function and 12 had biopsy proven membranous glomerulonephritis (WHO class V). The starting daily dose for MMF was 1.5 g to a maximum of 3 g. Patients were divided into: partial response, >or=50% decrease of baseline proteinuria; complete response, normal proteinuria levels (less than 0.3 g/24 h); flare, increase of at least 50% of the mean baseline proteinuria. All 20 SLE patients (100%) presented a 50% reduction of baseline proteinuria which was achieved in 8.2+/-3.3 months of MMF therapy, at a mean daily dose of 2.3+/-0.5 g. A significant decrease in 24-h protein excretion was observed compared to entry (3.47+/-1.26 vs. 1.33+/-0.67 g, P<0.0001) as well as a correspondent increase of serum albumin (3.2+/-0.4 vs. 3.7+/-0.4 mg/dl, P=0.02) and reduction of prednisone dose (33.7+/-20.0 to 18.6+/-14.1 mg/day, P=0.01). Complete response was observed in 11 SLE patients (55%) in 12.2+/-3.0 months of therapy with a significant decrease in proteinuria (P<0.0001), prednisone dose (P<0.0001) and an increase of serum albumin (P=0.003). Interestingly, initial proteinuria or serum albumin levels did not identify patients with complete response and those with partial response at the end of the study (P=0.543 and 0.657, respectively). Our pilot prospective study suggests that MMF appears to be effective in reducing severe persistent proteinuria in lupus glomerulonephritis, even in patients unresponsive to other immunosuppressive treatments.

Adult↗
PubMed2005

Proteinuria in South Asian children: prevalence and determinants.

Proteinuria in children is a marker of kidney disease and atherosclerosis, both which are known predictors of cardiovascular mortality. Recent evidence suggests that migrant South Asian populations living in the West may be at higher risk of kidney disease than native Caucasians. However, the determinants of proteinuria in South Asian children have not been explored. Previously, we reported ethnic variation in the prevalence of proteinuria in the adult population of Pakistan. However, it is not known whether ethnic predisposition to proteinuria appears during childhood or whether it is acquired later in life as a result of prolonged exposure to undiagnosed diabetes and hypertension. Analyses were based on a subset of data for 4977 children aged 5 to less than 15 years collected as part of the broad National Health Survey of Pakistan, conducted between 1990 and 1994. Proteinuria was defined as a dipstick positive for protein on a random urine sample. Ethnicity was reported as "mother-tongue", which is specific for each of the five major ethnic subgroups of Pakistan: Muhajir, Punjabi, Sindhi, Pashtun, and Baluchi. The overall prevalence (95% CI) of proteinuria in the children was 3.3% (2.7-3.9%). It was 6.2% in Sindhis, 3.6% in Muhajirs, 2.8% in Punjabis, 2.8% in Baluchis, and 1.0% in Pashtuns (p<0.001). In multivariable analyses, proteinuria was associated with greater height (p=0.007), urban dwelling (p=0.03), lower socioeconomic status (p=0.02), and certain ethnicities (p=0.005). The ethnic variation in proteinuria in South Asian children mirrors variation among ethnic groups in adults. This suggests variations in susceptibility or early exposure to causes of chronic kidney disease, rather than long-term exposure to undiagnosed diabetes or hypertension. Further studies are needed to determine factors in early life that may differentially predispose certain ethnic groups to proteinuria.

Adolescent↗
PubMed2005

Nephrotic range proteinuria and CD4 count as noninvasive indicators of HIV-associated nephropathy.

PURPOSE: Human immunodeficiency virus (HIV)-associated nephropathy is a common and serious cause of progressive renal insufficiency in patients with HIV, frequently presenting with nephrotic range proteinuria. The purpose of this study is to document the histopathologic diagnoses seen in HIV-positive patients with and without nephrotic range proteinuria and to evaluate the predictive value of both nephrotic range proteinuria and CD4 count in diagnosing HIV-associated nephropathy. METHODS: We performed a cross-sectional, single-center study of all 107 HIV-positive patients who had both a renal biopsy and urine protein measurement between 1995 and 2002. Nephrotic range proteinuria was defined as a urine protein-to-creatinine ratio > 3 or a 24-hour urine protein > 3 g. Clinical and laboratory characteristics of those patients with and without HIV-associated nephropathy were compared. Sensitivity, specificity, and positive and negative predictive values of nephrotic range proteinuria in the diagnosis of HIV-associated nephropathy were determined. RESULTS: Fifty-five biopsied patients had nephrotic range proteinuria, among whom 29 (53%) were diagnosed with HIV-associated nephropathy. Among the remaining patients, 12 had non-HIV-associated nephropathy focal segmental glomeruloscerlosis, 3 had membranoproliferative glomerulonephritis, 2 had AA Amyloid, 2 had diabetic nephropathy, and 7 had other diagnoses. Sensitivity, specificity, and positive and negative predictive values of nephrotic proteinuria in the diagnosis of HIV-associated nephropathy were 73%, 61%, 53%, and 79%, respectively. The patients with HIV-associated nephropathy had a significantly higher creatinine (8.2 mg/dL vs 2.5 mg/dL, P < .001) and a lower CD4 count (158 count/mm3 vs 349 count/mm3, P < .01) at the time of biopsy. Although significantly more patients with HIV-associated nephropathy had a CD4 count below 200 (P = .03), among those with a CD4 count below 200, 10 of 30 patients (33%) had diagnoses other than HIV-associated nephropathy. Injection drug use, presence of hepatitis C, and hypertension were not associated with HIV-associated nephropathy. CONCLUSION: Our results suggest that HIV patients with nephrotic range proteinuria warrant a kidney biopsy because the presence of nephrotic range proteinuria, even in the presence a low CD4 count, does not establish the diagnosis of HIV-associated nephropathy.

Adult↗
PubMed2006

Post-rapamycin proteinuria: incidence, evolution, and therapeutic handling at a single center.

We performed a retrospective study to evaluate the safety, incidence, and management of proteinuria in 31 renal transplant recipients converted to Rapamycin (RAPA). All patients received RAPA immediately after the cessation of the calcineurin inhibitor or the antiproliferative drug. No acute rejection episodes were seen after this regimen. Chronic allograft nephropathy (58.1%) and calcineurin inhibitor toxicity (51.6%), both biopsy-proven, were the major reasons to introduce RAPA. Post-RAPA proteinuria was defined as the appearance of urine protein excretion >300 mg/d or any further increase in protein among those who showed previously elevated levels. We observed an elevated incidence of proteinuria of 48.4%. It started at 5.3 +/- 2.5 months after the conversion and 60% occurred within 6 months. The proteinuria increased from a median of 200 mg/d to 1466 mg/d (P < .001). Age, gender, race, HLA mismatches, time to onset of RAPA, level of previous proteinuria, glomerular filtration rate, use of renin-angiotensin blockers, and etiology of chronic kidney disease were similar between the groups with or without proteinuria. Once it appeared, we suspended the drug in only 4 patients (26.7%), initiated or augmented the dosage of renin-angiotensin blockers in 26.7%, adjusted the RAPA dose in 20.1%, and did not perform a specific measure in 40% (6 of 15). At 15.6 +/- 12.7 months, 91% showed no further increase or reduction in proteinuria. We observed a high prevalence of proteinuria among renal transplant recipients converted to RAPA (48.4%). In addition, RAPA was suspended in only 4 patients and the proteinuria showed a tendency to stabilize or reduce over time.

Adult↗
PubMed2006

Proteinuria after conversion to sirolimus in renal transplant recipients.

Sirolimus (SRL) is a new, potent immunosuppressive agent. More recently, proteinuria has been reported as a consequence of sirolimus therapy, although the mechanism has remained unclear. We retrospectively examined the records of 25 renal transplant patients, who developed or displayed increased proteinuria after SRL conversion. The patient cohort (14 men, 11 women) was treated with SRL as conversion therapy, due to chronic allograft nephropathy (CAN) (n = 15) neoplasia (n = 8); Kaposi's sarcoma, Four skin cancers, One intestinal tumors, One renal cell carsinom) or BK virus nephropathy (n = 2). SRL was started at a mean of 78 +/- 42 (15 to 163) months after transplantation. Mean follow-up on SRL therapy was 20 +/- 12 (6 to 43) months. Proteinuria increased from 0.445 (0 to 1.5) g/d before conversion to 3.2 g/dL (0.2 to 12) after conversion (P = 0.001). Before conversion 8 (32%) patients had no proteinuria, whereas afterwards all patients had proteinuria. In 28% of patients proteinuria remained unchanged, whereas it increased in 68% of patients. In 40% it increased by more than 100%. Twenty-eight percent of patients showed increased proteinuria to the nephrotic range. Biopsies performed in five patients revealed new pathological changes: One membranoproliferative glomerulopathy and interstitial nephritis. These patients showed persistently good graft function. Serum creatinine values did not change significantly: 1.98 +/- 0.8 mg/dL before SRL therapy and 2.53 +/- 1.9 mg/dL at last follow-up (P = .14). Five grafts were lost and the patients returned to dialysis. Five patients displayed CAN and Kaposi's sarcoma. Mean urinary protein of patients who returned to dialysis was 1.26 (0.5 to 3.5) g/d before and 4.7 (3 to 12) g/d after conversion (P = .01). Mean serum creatinine level before conversion was 2.21 mg/dL and thereafter, 4.93 mg/dL (P = .02). Heavy proteinuria was common after the use of SRL as rescue therapy for renal transplantation. Therefore, conversion should be considered for patients who have not developed advanced CAN and proteinuria. The possibility of de novo glomerular pathology under SRL treatment requires further investigation by renal biopsy.

Adult↗